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J Appl Physiol (1985). 2019 Jan 1;126(1):193-201. doi: 10.1152/japplphysiol.00358.2018. Epub 2018 Nov 15.

Voluntary running protects against neuromuscular dysfunction following hindlimb ischemia-reperfusion in mice.

Author information

1
Department of Biochemistry and Molecular Genetics, Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine , Charlottesville, Virginia.
2
Center for Skeletal Muscle Research, Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine , Charlottesville, Virginia.
3
Department of Kinesiology, University of Georgia , Athens, Georgia.
4
Regenerative Bioscience Center, University of Georgia , Athens, Georgia.
5
Department of Medicine, Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine , Charlottesville, Virginia.
6
Institute of Cardiovascular Physiology, Heinrich Heine University of Düsseldorf , Düsseldorf , Germany.
7
Department of Pharmacology, Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine , Charlottesville, Virginia.
8
Department of Molecular Physiology and Biological Physics, Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine , Charlottesville, Virginia.

Abstract

Ischemia-reperfusion (IR) due to temporary restriction of blood flow causes tissue/organ damages under various disease conditions, including stroke, myocardial infarction, trauma, and orthopedic surgery. In the limbs, IR injury to motor nerves and muscle fibers causes reduced mobility and quality of life. Endurance exercise training has been shown to increase tissue resistance to numerous pathological insults. To elucidate the impact of endurance exercise training on IR injury in skeletal muscle, sedentary and exercise-trained mice (5 wk of voluntary running) were subjected to ischemia by unilateral application of a rubber band tourniquet above the femur for 1 h, followed by reperfusion. IR caused significant muscle injury and denervation at neuromuscular junction (NMJ) as early as 3 h after tourniquet release as well as depressed muscle strength and neuromuscular transmission in sedentary mice. Despite similar degrees of muscle atrophy and oxidative stress, exercise-trained mice had significantly reduced muscle injury and denervation at NMJ with improved regeneration and functional recovery following IR. Together, these data suggest that endurance exercise training preserves motor nerve and myofiber structure and function from IR injury and promote functional regeneration. NEW & NOTEWORTHY This work provides the first evidence that preemptive voluntary wheel running reduces neuromuscular dysfunction following ischemia-reperfusion injury in skeletal muscle. These findings may alter clinical practices in which a tourniquet is used to modulate blood flow.

KEYWORDS:

endurance exercise training; ischemia reperfusion; mitochondria; motor nerve; neuromuscular junction; oxidative stress; skeletal muscle

PMID:
30433863
PMCID:
PMC6383643
[Available on 2020-01-01]
DOI:
10.1152/japplphysiol.00358.2018

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